Search results for "kinase inhibitor"

showing 10 items of 414 documents

Cyclic pentapeptide cRGDfK enhances the inhibitory effect of sunitinib on TGF-β1-induced epithelial-to-mesenchymal transition in human non-small cell…

2020

AbstractIn human lung cancer progression, the EMT process is characterized by the transformation of cancer cells into invasive forms that migrate to other organs. Targeting to EMT-related molecules is emerging as a novel therapeutic approach for the prevention of lung cancer cell migration and invasion. Traf2- and Nck-interacting kinase (TNIK) has recently been considered as an anti-proliferative target molecule to regulate the Wnt signaling pathway in several types of cancer cells. In the present study, we evaluated the inhibitory effect of a tyrosine kinase inhibitor sunitinib and the integrin-αVβ3targeted cyclic peptide (cRGDfK) on EMT in human lung cancer cells. Sunitinib strongly inhib…

0301 basic medicineCell signalingIntegrinsLung NeoplasmsProtein ExpressionCancer TreatmentSmad ProteinsSignal transductionLung and Intrathoracic TumorsTyrosine-kinase inhibitorAdenosine Triphosphate0302 clinical medicineCarcinoma Non-Small-Cell LungCatalytic DomainAntineoplastic Combined Chemotherapy ProtocolsMedicine and Health SciencesSunitinibWnt Signaling PathwayWNT Signaling CascadeMultidisciplinarySunitinibChemistryQRWnt signaling pathwaySignaling cascadesDrug SynergismExtracellular MatrixMolecular Docking SimulationOncology030220 oncology & carcinogenesisMedicineCellular Structures and OrganellesSignal transductionResearch Articlemedicine.drugCell biologySignal InhibitionEpithelial-Mesenchymal TransitionCell Survivalmedicine.drug_classScienceSMAD signalingProtein Serine-Threonine KinasesResearch and Analysis MethodsPeptides CyclicTransforming Growth Factor beta103 medical and health sciencesCell Line TumorGene Expression and Vector TechniquesCell AdhesionBiomarkers TumormedicineHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionMolecular Biology TechniquesLung cancerMolecular BiologyA549 cellMolecular Biology Assays and Analysis TechniquesBiology and life sciencesCancers and NeoplasmsIntegrin alphaVbeta3medicine.diseaseNon-Small Cell Lung Cancer030104 developmental biologyTGF-beta signaling cascadeA549 CellsTNIKCancer cellCancer researchPLOS ONE
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Cancer combination therapy of the sesquiterpenoid artesunate and the selective EGFR-tyrosine kinase inhibitor erlotinib.

2017

Abstract Background The shift from cytotoxic to targeted chemotherapy led to improved treatment outcomes in oncology. Nevertheless, many cancer patients cannot be cured from their disease because of the development of drug resistance and side effects. Purpose There is an ongoing quest for novel compounds, which raised not only the interest in natural products but also in novel combination therapy regimens. Study design In this review, we report on the inhibition epidermal growth factor receptor (EGFR) by targeted small molecules and their combination with natural products from medicinal plants. Results The combination of erlotinib with artesunate leads to synergistic inhibition of cell grow…

0301 basic medicineCombination therapymedicine.medical_treatmentPharmaceutical ScienceArtesunateDrug resistancePharmacology03 medical and health scienceschemistry.chemical_compoundErlotinib Hydrochloride0302 clinical medicineIn vivoDrug DiscoveryAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansEpidermal growth factor receptorMolecular Targeted TherapyProtein Kinase InhibitorsPharmacologyChemotherapybiologybusiness.industryCancermedicine.diseaseArtemisininsErbB Receptors030104 developmental biologyComplementary and alternative medicinechemistryArtesunate030220 oncology & carcinogenesisbiology.proteinMolecular MedicineErlotinibbusinessmedicine.drugPhytomedicine : international journal of phytotherapy and phytopharmacology
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The emergence of drug resistance to targeted cancer therapies: Clinical evidence.

2019

For many decades classical anti-tumor therapies included chemotherapy, radiation and surgery; however, in the last two decades, following the identification of the genomic drivers and main hallmarks of cancer, the introduction of therapies that target specific tumor-promoting oncogenic or non-oncogenic pathways, has revolutionized cancer therapeutics. Despite the significant progress in cancer therapy, clinical oncologists are often facing the primary impediment of anticancer drug resistance, as many cancer patients display either intrinsic chemoresistance from the very beginning of the therapy or after initial responses and upon repeated drug treatment cycles, acquired drug resistance deve…

0301 basic medicineDrugCancer Researchmedicine.drug_classmedicine.medical_treatmentmedia_common.quotation_subjectTranslational researchApoptosisDrug resistanceMonoclonal antibodyBioinformatics03 medical and health sciences0302 clinical medicineNeoplasmsmedicineHumansPharmacology (medical)Hedgehog ProteinsEpigeneticsProtein Kinase Inhibitorsmedia_commonPharmacologyChemotherapybusiness.industryCancerImmunotherapyProtein-Tyrosine Kinasesmedicine.disease030104 developmental biologyInfectious DiseasesOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbusinessProteasome InhibitorsDrug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
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Kinase Inhibitors in Multitargeted Cancer Therapy

2017

The old-fashioned anticancer approaches, aiming in arresting cancer cell proliferation interfering with non-specific targets (e.g. DNA), have been replaced, in the last decades, by more specific target oriented ones. Nonetheless, single-target approaches have not always led to optimal outcomes because, for its complexity, cancer needs to be tackled at various levels by modulation of several targets. Although at present, combinations of individual single-target drugs represent the most clinically practiced therapeutic approaches, the modulation of multiple proteins by a single drug, in accordance with the polypharmacological strategy, has become more and more appealing. In the perspective of…

0301 basic medicineDrugNiacinamideIndolesPyridinesmedia_common.quotation_subjectPharmacologyBioinformaticsBiochemistryReceptor tyrosine kinase03 medical and health sciencesCrizotinibPiperidinesMultitargeted drugs anticancer agents polypharmacology tyrosine kinase receptors oncogene addiction tumor microenvironment FDA-approved drugsNeoplasmsDrug DiscoverymedicineSunitinibHumansAnilidesPyrrolesProtein Kinase Inhibitorsmedia_commonPharmacologyTumor microenvironmentbiologybusiness.industryPhenylurea CompoundsOrganic ChemistryImidazolesCancerReceptor Protein-Tyrosine KinasesSorafenibmedicine.diseaseOncogene AddictionSettore CHIM/08 - Chimica FarmaceuticaClinical trialPyridazines030104 developmental biologyMechanism of actionbiology.proteinImatinib MesylateQuinazolinesMolecular MedicinePyrazolesmedicine.symptombusinessTyrosine kinase
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FGFR a promising druggable target in cancer: Molecular biology and new drugs.

2017

Abstract: Introduction: The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered: This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion: Most of the TKR share …

0301 basic medicineFibroblast Growth FactorDruggabilityFibroblast growth factorTyrosine-kinase inhibitorReceptor tyrosine kinase0302 clinical medicineNeoplasmsFGFR inhibitorsFGFMolecular Targeted TherapyCancerCancer; FGF; FGFR; FGFR inhibitors; Drug Resistance Neoplasm; Fibroblast Growth Factors; Gene Fusion; Humans; Molecular Targeted Therapy; Mutation; Neoplasms; Protein Kinase Inhibitors; Receptors Fibroblast Growth Factor; Signal Transduction; Hematology; Oncology; Geriatrics and GerontologybiologyFGFRHematologyFGFR inhibitorOncologyFibroblast growth factor receptor030220 oncology & carcinogenesisembryonic structuresSignal transductionbiological phenomena cell phenomena and immunityGene FusionHumanSignal Transductionmusculoskeletal diseasesanimal structuresmedicine.drug_classProtein Kinase Inhibitor03 medical and health sciencesmedicineHumansProtein Kinase InhibitorsCancer; FGF; FGFR; FGFR inhibitorsbusiness.industryCancermedicine.diseaseMolecular biologyReceptors Fibroblast Growth FactorFibroblast Growth Factors030104 developmental biologyDrug Resistance NeoplasmCancer cellMutationbiology.proteinNeoplasmHuman medicineGeriatrics and GerontologybusinessCritical reviews in oncology/hematology
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Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis

2016

Background Obesity has tremendous impact on the health systems. Its epigenetic bases are unclear. MacroH2A1 is a variant of histone H2A, present in two alternatively exon-spliced isoforms macroH2A1.1 and macroH2A1.2, regulating cell plasticity and proliferation, during pluripotency and tumorigenesis. Their role in adipose tissue plasticity is unknown. Results Here, we show evidence that macroH2A1.1 protein levels in the visceral adipose tissue of obese humans positively correlate with BMI, while macroH2A1.2 is nearly absent. We thus introduced a constitutive GFP-tagged transgene for macroH2A1.2 in mice, and we characterized their metabolic health upon being fed a standard chow diet or a hig…

0301 basic medicineGenetically modified mouseCyclin-Dependent Kinase Inhibitor p21macroh2a1.2TransgeneAdipose tissueAdipose tissueMice TransgenicBiologyCarbohydrate metabolismDiet High-FatBody Mass IndexCell LineHistones03 medical and health sciencesMiceHistone variantGeneticsAnimalsHumansInsulinEpigeneticsAdipose tissue Histone variants Obesity macroh2a1.2ObesityTranscription factorPancreasMolecular BiologyUncoupling Protein 1SkinHistone variantsAdipogenesisResearchCell DifferentiationGlucose Tolerance TestMolecular biologyCell biologyMice Inbred C57BL030104 developmental biologyPhenotypeLiverMetabolic EngineeringAdipogenesisDNA methylationAdipose tissue; Histone variants; macroh2a1.2; Obesity; Molecular Biology; Genetics
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Synthesis, antitumor activity and CDK1 inhibiton of new thiazole nortopsentin analogues

2017

A new series of thiazole nortopsentin analogues was conveniently synthesized with fair overall yields. The antiproliferative activity of the new derivatives was tested against different human tumor cell lines of the NCI full panel. Four of them showed good antitumor activity with GI(50) values from micro to nanomolar level. The mechanism of the antiproliferative effect of these derivatives, was pro-apoptotic, being associated with externalization of plasma membrane phosphatidylserine and DNA fragmentation. The most active and selective of the new thiazoles confined viable cells in G2/M phase and markedly inhibited in vitro CDK1 activity. (C) 2017 Elsevier Masson SAS.

0301 basic medicineIndolesCell SurvivalStereochemistryMolecular ConformationNortopsentin analogues3-b]pyridinesAntineoplastic AgentsApoptosisMarine alkaloids Nortopsentin analogues Antiproliferative activity Apoptosis CDK1 inhibitors Thiazolyl-1H-pyrrolo[23-b]pyridinesAntiproliferative activity01 natural sciencesStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compoundMarine alkaloidsCDC2 Protein KinaseDrug DiscoveryHumansThiazoleProtein Kinase InhibitorsCell ProliferationPharmacologyCyclin-dependent kinase 1Dose-Response Relationship DrugMarine alkaloids; Nortopsentin analogues; Antiproliferative activity; Apoptosis; CDK1 inhibitors; Thiazolyl-1H-pyrrolo[2; 3-b]pyridines010405 organic chemistryOrganic ChemistryImidazolesGeneral MedicinePhosphatidylserineThiazolyl-1H-pyrrolo[2Settore CHIM/08 - Chimica FarmaceuticaCyclin-Dependent KinasesIn vitro0104 chemical sciencesCDK1 inhibitors030104 developmental biologyMembranechemistryCell cultureApoptosisMCF-7 CellsDNA fragmentationCaco-2 CellsDrug Screening Assays Antitumor
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Anticancer potential of novel α,β-unsaturated γ-lactam derivatives targeting the PI3K/AKT signaling pathway.

2021

Abstract Six recently synthesized alkyl (Z)-2-(2-oxopyrrolidin-3-ylidene)acetates were evaluated for their potential as cytotoxic and anticancer agents. All compounds were tested in the ERα positive MCF-7, triple negative MDA-MB-231, and Her2+ SKBR-3 breast cancer cell lines. The most lipophilic derivatives, bearing the 4-isopropylphenyl (2) or 4-tert-butylphenyl (3) group at the γ-lactam nitrogen, proved to be cytotoxic against all the cancer cell lines tested (IC50 values ranging from 18 to 63 μM), exerting their greatest activity in SKBR-3 cells, with IC50 values of 33 and 18 μM, respectively. Biological studies showed that the cytotoxic effects of 2 and 3 are accompanied by apoptotic de…

0301 basic medicineLactamsCell SurvivalAntineoplastic AgentsApoptosisBreast NeoplasmsBiochemistry03 medical and health scienceschemistry.chemical_compoundPI3K/AKT signaling pathwayPhosphatidylinositol 3-Kinases0302 clinical medicinebreast cancerCytotoxic T cellHumansα-methylene-γ-lactamsαβ-unsaturated lactamsCytotoxicityPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsPharmacologychemistry.chemical_classificationBiological ProductsMolecular StructureChemistryCell growthAkt/PKB signaling pathwayCell CycleEpithelial Cells030104 developmental biologyEnzymeGene Expression RegulationApoptosis030220 oncology & carcinogenesisCancer researchLactamcytotoxicityFemaleProto-Oncogene Proteins c-aktBiochemical pharmacology
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PI3K inhibition reduces murine and human liver fibrogenesis in precisioncut liver slices

2019

Background: Liver fibrosis results from continuous inflammation and injury. Despite its high prevalence worldwide, no approved antifibrotic therapies exist. Omipalisib is a selective inhibitor of the PI3K/mTOR pathway that controls nutrient metabolism, growth and proliferation. It has shown antifibrotic properties in vitro. While clinical trials for idiopathic pulmonary fibrosis have been initiated, an in-depth preclinical evaluation is lacking. We evaluated omipalisib's effects on fibrogenesis using the ex vivo model of murine and human precision-cut tissue slices (PCTS).Methods: Murine and human liver and jejunum PCTS were incubated with omipalisib up to 10 mu M for 48 h. PI3K pathway act…

0301 basic medicineLiver CirrhosisMalePrecision-cut tissue slicesPROGRESSIONPharmacologyBILIARYBiochemistryPI3KGSK2126458JejunumMicePhosphatidylinositol 3-Kinases0302 clinical medicineAdenosine TriphosphateFibrosisFIBROSIShealth care economics and organizationsPhosphoinositide-3 Kinase InhibitorsSulfonamidesPyridazinesmedicine.anatomical_structureJejunumTARGET030220 oncology & carcinogenesisToxicityQuinolinesPhosphorylationmedicine.symptomATP Binding Cassette Transporter Subfamily BLiver fibrosisEARLY-ONSETInflammation03 medical and health sciencesmedicineAnimalsHumansOmipalisibProtein kinase BPI3K/AKT/mTOR pathwayPharmacologybusiness.industryCUT LIVERmedicine.diseaseMice Inbred C57BLMODEL030104 developmental biologybusinessMATRIXEx vivoBiochemical Pharmacology
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Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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